Potential utility of PPARγ agonists in targeting chronic myeloid leukemia stem cells.

Basma Atef, Shaimaa El-Ashwah, Layla M Saleh, Hanan Gawish, Mohamed Mabed

Registry-linked trialAbstract read

In one paragraph

Article in Annals of hematology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04883125 (Potential Utility of Peroxisome Proliferator-activated Receptor Gamma Agonists in the Eradication of Chronic Myeloid Leukemia Stem Cells), which is not on this map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT04883125 phase2completednot on this map

Potential Utility of Peroxisome Proliferator-activated Receptor Gamma Agonists in the Eradication of Chronic Myeloid Leukemia Stem Cells: Myth or Truth?

TypeinterventionalSponsorMansoura UniversityRan2018 to 2021Enrolled90ConditionsChronic Myelogenous Leukemia, BCR-ABL Positive, CML, Chronic PhaseArmsPioglitazone 15mg

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Basma AtefHematology Unit, Internal Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.

Shaimaa El-AshwahHematology Unit, Internal Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.

Layla M SalehClinical Pathology Department, Faculty of Medicine, Hematology Unit, Mansoura University, Mansoura, Egypt.

Hanan GawishDiabetes & Endocrinology Unit, Internal Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.

Mohamed MabedHematology Unit, Internal Medicine Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt. mohmabed@mans.edu.eg.ORCID http://orcid.org/0000-0002-5832-3561

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tyrosine kinase inhibitors (TKIs) have transformed the treatment of chronic myeloid leukemia (CML), yet persistent leukemia stem cells (LSCs) remain a barrier to cure. PPARγ agonists like pioglitazone have been proposed to enhance eradication of LSCs when used alongside TKIs. This study investigated the impact of adding pioglitazone to imatinib therapy in 26 newly diagnosed chronic-phase CML patients. Patients received imatinib (400 mg) plus pioglitazone (15 mg) daily for six months, with follow-up extending to 60 months. Treatment responses and adverse events were recorded, and expression levels of CITED2 and HIF2α genes were measured before and after therapy, compared to a control group of 52 matched patients treated with imatinib alone. The combination therapy showed improved early cytogenetic and molecular responses, though long-term outcomes were not significantly different. Significant reductions in median CITED2 (from 276.3 to 2.6; P = 0.005) and HIF2α (from 2.7 to 1; P = 0.026) expression were observed post-treatment. These results suggest that pioglitazone may enhance early molecular response and suppress LSC-associated genes, but further research is needed to confirm its long-term benefit and clarify the role of PPARγ modulation in CML management. Clinical Trial Number: NCT04883125.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveNeoplastic Stem CellsPPAR gammaPPAR-gamma AgonistsAdultAgedBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1FemaleHumansImatinib MesylateMaleMiddle AgedPioglitazoneRepressor ProteinsBasic Helix-Loop-Helix ProteinsCITED2 protein, humanEndothelial PAS Domain-Containing Protein 1Imatinib MesylatePioglitazonePPAR gammaPPAR-gamma AgonistsRepressor ProteinsThiazolidinedionesTrans-ActivatorsChronic myeloid leukemiaCITED2 geneHIF2α geneLeukemic stem cellsPioglitazonePPARγ agonists

Identifiers

PMID41735647

DOI10.1007/s00277-026-06795-7

PMCPMC12932272

What OpenQuestion holds

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LicenceCC BY

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Registered trials

NCT04883125ClinicalTrials.gov

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.